eMedicine Specialties > Emergency Medicine > Dermatology

Dermatitis, Atopic

Jamie Alison Edelstein, MD, Staff Physician, Department of Emergency Medicine, State University of New York, Kings County Hospital Center
Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Updated: Jun 30, 2009

Introduction

Background

Eczema, or atopic dermatitis, is a common inflammatory disease of the skin. The condition often has its start in childhood and follows a variable and sometimes unremitting course. Historically, this disease has been considered a part of a triad of "atopy" that included asthma and allergic rhinitis, though this association has recently come into question. Although not a cause of significant mortality, the visible and chronic nature of eczema can be a source of emotional stress.

Pathophysiology

The precise mechanism for the development of eczema is unknown. Whether the clinical manifestations of atopic dermatitis (AD) are the result of violation of the epidermis and the subsequent contact between environmental irritants and immune cells, or the reverse sequence, is debatable. Nonetheless, the epidermis is the first line of defense between the body and the environment and, when intact, shields the body from a variety of irritants, allergens, and microbes. This barrier, which is maintained by differentiated keratinocytes and structural proteins, can be compromised by inheritance, trauma, decreased humidity, change in pH, and infection.
 
Atopic skin additionally has diminished ability to maintain water; this dry skin leads to scratching, which further contributes to the release of proinflammatory mediators. Eczema is a biphasic T-cell – mediated disease: TH2 is more prevalent in the acute phase, and TH1 predominates in the chronically affected skin.¹ Patients with atopic dermatitis have elevated serum IgE levels, peripheral eosinophilia, and overall greater numbers of immune mediators and cytokines.

Frequency

Atopic dermatitis is the most common inflammatory skin disease in children, affecting up to 17% of the pediatric population in the United States, with increasing prevalence over the past several decades.

United States

Prevalence of atopic dermatitis ranges from approximately 7-17% in children.² A small percentage of affected children will have the disease into adulthood.

International

Studies in Japan and Northern Europe have found similar prevalence, with industrialized and westernized nations noting increasing trends of patients with atopic dermatitis.

Mortality/Morbidity

Mortality is not associated with atopic dermatitis. The impact of eczema is hard to measure but has real personal, social, and financial consequences. The burden includes but is not limited to professional fees, hospitalization, pain/suffering, social isolation, poor self-esteem, and work and/or school performance or absence. Additionally, patients suffering from atopic dermatitis are prone to bacterial superinfection.

Sex

Data shows a slightly increased prevalence of atopic dermatitis in female children.

Age

Atopic dermatitis predominantly affects infants and young children. Eczema is apparent in the first year of life in 60% of cases, and its onset is before 5 years in 75% of cases.³ Onset of eczematous appearing disease in adulthood should lead the physician to consider another diagnosis.

A triphasic course of atopic dermatitis across the lifespan has been proposed. Phase I develops before IgE sensitization has taken place and occurs mostly in infants who are likely genetically predisposed to the disease. Phase II involves IgE sensitization to food, environmental antigens, or both. Phase III is the product of chronic scratching and is characterized by the formation of IgE autoantibodies against proteins of keratinocytes and endothelial cells.

Clinical

History

The hallmarks of atopic dermatitis are intense pruritus, chronic eczematous skin lesions, and epidermal thickening and hypertrophy.

• The emergency physician often is the first to diagnose atopic dermatitis. The most common presentation is that of infants, usually younger than 6 months, brought in by their parents for a persistent rash. Before coming to the ED, the parents may have tried a number of over-the-counter and home remedies. Parents usually report that the rash has waxed and waned for months with a history of dry skin since birth.
• Clinicians should inquire about a family history of asthma, hay fever, allergy, and other atopic diseases. Patients with pertinent medical or family history of such disease tend to have a worse prognosis.
• Parents may also give a history of poor sleep or increased irritability in the patients, which is due to the desire to scratch the skin during sleep. Atopic dermatitis begins with intense pruritus, leading the patient to scratch, which results in the characteristic rash.
• Atopic dermatitis typically is not associated with fever or other constitutional symptoms, and the presence of these should prompt the clinician to look for bacterial superinfection.

Physical

Atopic dermatitis is a spectrum of disease that varies in presentation, severity, and distribution. Eczema defies a simple definition as the disease has differing characteristics depending on the age of the patient and the stage of the disease course.

• Lesions may be acute, subacute, or chronic, each with a characteristic appearance. Lesions from one stage can convert into another stage at any time due to processes such as manipulation, irritation, allergy, or infection.
  • Acute lesions are intensely itchy and present as vesicles and blisters with intense redness.
  • Subacute disease is characterized by slight-to-moderate itching, pain, stinging, burning and redness, scaling, and fissuring of the skin with a parched and scalded appearance.
  • Chronic eczematous inflammation demonstrates thickened skin, accentuated skin lines, excoriations, and fissuring accompanying a moderate-to-intense itch.
• The pattern of skin manifestations also differs across the lifespan.
  • In infantile atopic dermatitis, pruritic, red, scaly, and crusted lesions are typically found on the extensor surfaces and cheeks or scalp, with severe cases possibly presenting with vesicles, serous exudates, or crusting. The diaper area is protected and usually spared.
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    Irritation around mouth of an infant with atopic dermatitis.

    
    
  • The lesions in the childhood stage have less exudation; the skin often demonstrates lichenified plaques in a flexural distribution, commonly antecubital and popliteal fossae, volar aspect of the wrists, ankles, and neck.
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    Flexural involvement in childhood atopic dermatitis.

    
    
  • Adult eczema has a similar distribution to that in childhood atopic dermatitis but is increasingly localized and lichenified with thickened skin, increased skin markings, and excoriated and fibrotic papules.
• Certain characteristic patterns are worth mentioning.
  • Eczema that appears as one or several coin-shaped plaques is called nummular eczema.
  • Plaques with prominent skin lines are referred to as lichen simplex chronicus. These lesions are characterized by intense pruritus that ceases when pain replaces itch.

Diagnosis of atopic dermatitis is made by observing representative clinical features of the disease. The Hanifin and Rajka diagnostic criteria, which consist of 4 major and 23 minor criteria has traditionally been used, but it is time consuming and not manageable. The UK working group on atopic dermatitis has the following criteria for diagnosis, which has been most extensively validated in clinical trials.⁴ Evidence of itchy skin with 3 more of the following:

• History of skin crease involvement
• Presence of generally dry skin within in the past year
• Symptoms in a child beginning before the age of 2 years
• Visible involvement of dermatitis involving flexural surfaces

The complete Hanifin and Rajka criteria are included below:

• Major criteria (need 3 or more)
  • Pruritus
  • Typical morphology and distribution
  • Flexural lichenification in adults
  • Facial and extensor involvement in infants and children
  • Dermatitis - Chronically or chronically relapsing
  • Personal or family history of atopy (asthma, allergic rhinitis, atopic dermatitis)
• Minor criteria (need 3 or more)
  • Cataracts
  • Cheilitis
  • Conjunctivitis - Recurrent
  • Eczema - Perifollicular accentuation
  • Facial pallor or erythema
  • Food intolerance
  • Hand dermatitis - Nonallergic
  • Ichthyosis
  • IgE - Elevated
  • Immediate (type I) skin test reactivity
  • Infections (cutaneous)
  • Dennie-Morgan infraorbital fold
  • Itching when sweating
  • Keratoconus
  • Keratosis pilaris
  • Nipple dermatitis
  • Orbital darkening
  • Palmar hyperlinearity
  • Pityriasis alba
  • White dermographism
  • Wool intolerance
  • Xerosis

Causes

Atopic dermatitis is a complex genetic disease that results from an array of gene-gene and gene-environment interactions. Most experts believe that atopic dermatitis has a genetic basis. This is supported by twin studies and chromosome studies that suggest the trait might be inherited via a maternal gene located on chromosome 11. Clinical studies have also shown a higher risk of atopy in children with maternal atopy than in children with paternal atopy.⁵

Two theories have been proposed to explain the manifestations of atopic dermatitis. Atopic dermatitis was traditionally thought to be caused by an innate immunologic disturbance leading to IgE sensitization, which later results in disruption of the epithelial barrier, though this supposed mechanism is falling out of favor. Alternatively, it is thought that skin breakdown precedes the inflammatory process and an intrinsic epithelial cell defect leads to barrier disruption of the skin and that immunologic imbalance is an "epiphenomenon".¹ Genetic defects in filaggrin, a group of structural proteins, have been cited as a major cause of atopic dermatitis.^6,7 The upregulation of a protease stratum corneum chymotryptic enzyme is also being investigated in the cause of atopic dermatitis.

Chronic eczema is a disease that is somewhat behaviorally mediated. Skin thickening and plaque formation is dependent on habitual scratching.

Differential Diagnoses

Workup

Laboratory Studies

Laboratory testing, including IgE levels, is not necessary or recommended in the evaluation of suspected atopic dermatitis.

Procedures

• Pathologic findings of biopsy samples include spongiosis with a severely damaged stratum corneum, with hyperproliferation in advanced cases.
• Histological studies show an inflammatory infiltrate consisting of memory predominantly CD4 T lymphocytes. Chronic lesions also display increased mast cells, eosinophils, and IgE-bearing Langerhans cells.

Treatment

Emergency Department Care

Many patients with atopic dermatitis (AD) present to the ED during acute exacerbation. Therapy is targeted toward alleviation of pruritus and prevention of scratching. ED physicians must also look for signs and symptoms of bacterial superinfection and treat accordingly.

Practice guidelines on the management of atopic dermatitis are available from the Joint Task Force on Practice Parameters for Allergy and Immunology.⁸

• Skin care
  • In the acute setting patients should be instructed to bathe once-to-twice daily using mild soaps (eg, Dove). There is no preference over showers or baths, whichever makes the patient most comfortable.
  • The patient should dry quickly and immediately (within 3 min) lubricate the skin. Many creams and lotions are available, and the optimal one is the greasiest the patient can tolerate.
  • Creams (eg, Eucerin, Cetaphil) are preferred over lotions, as they have lower or no water content and will not evaporate off of the skin during the day. Parents may use petroleum jelly on infants, but most children and adults will not tolerate the texture.
• Topical steroids
  • Acute attacks should be treated by mid-high strength topical steroids for up to 2 weeks. Medium-to-high potency topical steroids should not be used on the face or neck area because of the potential adverse effects. These are preferred over low-mid strength medications, as they better control exacerbations. Patients should apply the ointment within 5 minutes of twice-daily bathing.
  • Inform the patient about adverse effects of topical steroids (eg, atrophy, hypopigmentation, striae, telangiectasia, thinning of the skin).
• Antihistamines: Physicians have been prescribing antihistamines for years to control the pruritus associated with acute atopic dermatitis. Little evidence exists that antihistamines help with the itching in an awake patient; however, the use of sedating antihistamines is supported to control scratching while the patient is asleep.⁹
• Systemic steroids: The use of systemic steroids in the treatment of acute exacerbation of atopic dermatitis is controversial. Most authors reserve oral prednisone (at least 20 mg/d for 7 d) for the most severe cases, although it seems the disease quickly relapses once the medication is discontinued. Patients also tend to discontinue topical steroid creams and other treatment as they feel better, which contributes to the relapse after oral steroids are done.
• Topical calcineurin inhibitors: Topical calcineurin inhibitors (pimecrolimus 1% and tacrolimus 0.03%, 0.1%) are available for patients older than 2 years. These medications may be used all over skin surfaces (including face, neck, and hairline) because they do not have the side effects seen with topical steroids. Evidence supports the twice-daily use of these creams during acute exacerbation of atopic dermatitis, and some evidence exists to support use up to 4 years. The long-term side effects (including the possibility of increased risk for malignancy) have not fully been elucidated. For these reasons, the US Food and Drug Administration (FDA) does not recommend long-term use yet. Side effects of tacrolimus include burning and stinging on broken skin.
• Oral immunosuppressive agents: Patients with refractory atopic dermatitis may benefit from oral immunosuppressive agents, such as cyclosporine A. This medication is effective in treating severe atopic dermatitis in the acute setting. It is not recommended for long-term use.
• Phototherapy with PUVA, UVA, or UVB is successful in controlling atopic dermatitis but is expensive and may lead to increased risk of melanoma and nonmelanoma skin cancer. Studies evaluating the role of several proposed disease-modifying agents continue to be conducted. Results of studies on IL-4 neutralizing antibody and mast cell depleters are promising, whereas the evidence for probiotics,^10,11 primrose oil, sodium cromolyn, topical caffeine, and dietary exclusion is inconclusive and requires more research.

Consultations

In cases of uncertain diagnosis or severe atopic dermatitis that is resistant to conventional therapy, patients may be referred to a specialist such as a dermatologist or an allergist.

Medication

Drug regimens for eczema should be tailored to the individual patient to reduce the frequency and severity of exacerbations.

Topical steroids

Topical steroids are very effective when used in the induction of remission and in the acute exacerbation of atopic dermatitis.

Low-to-medium potency steroids should be used routinely, with medium-to-high potency steroids for more severe rashes.

Triamcinolone (Aristocort)

A medium potency topical steroid. Treats inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Dosing

Adult

Apply bid to affected area

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; fungal, viral, and bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

A percentage of topical drug might be absorbed systemically; if application is repeated, there may be some systemic effects of the corticosteroids

Hydrocortisone (CortaGel, Cortaid, Dermacort, Westcort)

An example of a low-potency topical steroid available OTC. An adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. Has mineralocorticoid and glucocorticoid effects resulting in anti-inflammatory activity.

Dosing

Adult

Apply bid to affected areas

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; viral, fungal, and bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Prolonged use, applying over large surface areas, application of potent steroids, and using occlusive dressings may increase systemic absorption of corticosteroids and may cause Cushing syndrome, reversible HPA axis suppression, hyperglycemia, and glycosuria

Topical calcineurin Inhibitors

Topical immune suppressants that block early T-cell activation, degranulation of mast cells, and multiple cytokines.

Pimecrolimus (Elidel cream)

First nonsteroid cream approved in the US for mild-to-moderate atopic dermatitis. Derived from ascomycin, a natural substance produced by fungus Streptomyces hygroscopicus var ascomyceticus. Selectively inhibits production and release of inflammatory cytokines from activated T cells by binding to cytosolic immunophilin receptor macrophilin-12. The resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release. Cutaneous atrophy was not observed in clinical trials, a potential advantage over topical corticosteroids. Indicated only after other treatment options have failed.

Dosing

Adult

Apply topically to affected areas bid, short-term and intermittent use only

Pediatric

<2 years: Not established
>2 years: Administer as in adults, short-term and intermittent use only

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Potential exacerbation of existing infection at site of application; may cause burning and irritation; caution with conditions that suppress the immune system (eg, AIDS, cancer); possible risk of lymph node or skin cancer based on animal studies and a small number of patients; may increase risk of viral infections; other adverse effects include headache, sore throat, flulike symptoms, fever, and cough

Tacrolimus (Protopic)

The mechanism of action of tacrolimus in atopic dermatitis is not known. Reduces itching and inflammation by suppressing the release of cytokines from T cells. Also inhibits transcription for genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha, all of which are involved in the early stages of T-cell activation. Additionally, may inhibit release of preformed mediators from skin mast cells and basophils, and downregulate expression of FCeRI on Langerhans cells. Can be used in patients as young as 2 years. Drugs of this class are more expensive than topical corticosteroids. Available as an ointment in concentrations of 0.03% and 0.1%. Indicated only after other treatment options have failed.

Dosing

Adult

Apply thin layer to affected skin areas bid and rub in gently and completely; continue treatment for 1 wk after clearing of signs and symptoms; use short-term and intermittent use only

Pediatric

<2 years: Not established
2-15 years: Apply 0.03% ointment bid to affected area(s)
>15 years: Administer as in adults; use short-term and intermittent use only

Interactions

None reported

Contraindications

Documented hypersensitivity to tacrolimus or components of ointment

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Patients may experience a burning sensation during first few days of application; skin can become photosensitive, and patients should be cautioned about exposure to direct or artificial sunlight and to use sunscreen; safety and efficacy in infected atopic dermatitis is not known; application under occlusion, which may promote systemic exposure, has not been evaluated (do not use tacrolimus ointment with occlusive dressings); absorption of tacrolimus following topical applications of tacrolimus ointment is minimal (relative to systemic administration), but tacrolimus is excreted in human milk and, thus, a decision should be made whether to discontinue breastfeeding or to discontinue drug, taking into account importance of drug to mother (potential for serious adverse reactions in breastfeeding infants from tacrolimus should also be a concern)
Caution with conditions that suppress the immune system (eg, AIDS, cancer); possible risk of lymph node or skin cancer based on animal studies and a small number of patients; may increase risk of viral infections; other adverse effects include headache, sore throat, flulike symptoms, fever, and cough

Oral immunosuppressive agents

For use in severe refractory atopic dermatitis.

Cyclosporine (Neoral, Sandimmune)

An 11-amino acid cyclic peptide and natural product of fungi. Acts on T-cell replication and activity.
Specific modulator of T-cell function and an agent that depresses cell-mediated immune responses by inhibiting helper T-cell function. Preferential and reversible inhibition of T lymphocytes in G0 or G1 phase of cell cycle suggested.
Binds to cyclophilin, an intracellular protein, which, in turn, prevents formation of interleukin 2 and the subsequent recruitment of activated T cells.
Has about 30% bioavailability, but there is marked interindividual variability. Specifically inhibits T-lymphocyte function with minimal activity against B cells. Maximum suppression of T-lymphocyte proliferation requires that drug be present during first 24 h of antigenic exposure.
Suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions (eg, delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, and graft-vs-host disease) for a variety of organs.

Dosing

Adult

5 mg/kg/d PO qd

Pediatric

Not established

Interactions

Carbamazepine, phenytoin, isoniazid, rifampin, and phenobarbital may decrease cyclosporine concentrations; azithromycin, itraconazole, nicardipine, ketoconazole, fluconazole, erythromycin, verapamil, grapefruit juice, diltiazem, aminoglycosides, acyclovir, amphotericin B, and clarithromycin may increase cyclosporine toxicity; acute renal failure, rhabdomyolysis, myositis, and myalgias increase when taken concurrently with lovastatin; methylprednisolone and cyclosporine mutually inhibit one another resulting in increased plasma levels of each drug

Contraindications

Documented hypersensitivity; uncontrolled hypertension or malignancies; do not administer concomitantly with PUVA or UVB radiation in psoriasis since it may increase risk of cancer

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Evaluate renal and liver functions often by measuring BUN, serum creatinine, serum bilirubin and liver enzymes; may increase risk of infection and lymphoma; reserve IV use only for those who cannot take PO

Antihistamines

Used for the sedating effects. Help to prevent scratching during sleep.

Hydroxyzine hydrochloride (Atarax, Vistaril)

Antagonizes H1-receptors in the periphery. Also may suppress histamine activity in the subcortical region of the CNS. A sedating antihistamine.

Dosing

Adult

25-50 mg PO q4-6h prn

Pediatric

0.5 mg/kg PO q4-6h prn

Interactions

CNS depression may increase with alcohol or other CNS depressants

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Associated with clinical exacerbations of porphyria (may not be safe for porphyric patients); ECG abnormalities (alterations in T waves) may occur; may cause drowsiness

Follow-up

Further Inpatient Care

• Few patients with atopic dermatitis will require hospitalization. Patients with cellulitis or severe secondary infection may require intravenous antibiotics and sedation.

Further Outpatient Care

• Atopic dermatitis is chronic and relapsing. The main goal of treatment is control of the disease, not a cure. Patient education about management of flare and recognition of superinfection is paramount.

Inpatient & Outpatient Medications

• Few patients with atopic dermatitis will require hospitalization. Patients with cellulitis or severe secondary infection may require intravenous antibiotics and sedation.

Deterrence/Prevention

• Breastfeeding has indisputable benefits in infant nutrition, but no strong evidence suggests a protective effect against the development of atopic dermatitis, even in children with a family positive history.¹²
• The mainstay of treatment of atopic dermatitis is prevention of outbreaks. Patients should continue to take short showers/baths followed by immediate hydration of skin with emollients even during rash-free times. They should also continue to avoid any triggers that may exacerbate atopic dermatitis.

Complications

• Excoriations secondary to itch predispose to infection and can be recognized by the accumulation of serum, crust, and purulent material. Development of vesicle and/or pustules in patients with known atopic dermatitis should initiate a search for bacterial or viral superinfection; appropriate antibiotics or antivirals should be started immediately. Patients with atopic dermatitis are uniquely susceptible to herpes simplex, which may occasionally progress to a Kaposi’s varicelliform eruption; physicians and patients should be particularly vigilant for this condition. This rare complication is characterized by generalized involvement, systemic toxicity, and even death. In these cases, the patient should be treated with oral acyclovir and monitored closely. Topical corticosteroids and/or occlusive dressings are best, at least temporarily, discontinued.
• Exfoliative erythroderma is another rare complication, occurring in less than 1% of  patients with atopic dermatitis. Exfoliative erythroderma demonstrates a marked progression caused by widespread Staphylococcus aureus or herpes simplex superinfection and can be life threatening if it is complicated by high-output cardiac failure and heat loss.
• Atrophy or striae occur if fluorinated corticosteroids are used on the face or in skin folds.
• Systemic absorption of steroids may occur if large areas of skin are treated, particularly if high-potency medications and occlusion are combined.

Prognosis

• About 90% of patients with atopic dermatitis have spontaneous resolution by puberty.
• Adults who continue to have atopic dermatitis usually have localized dermatitis (eg, chronic hand or foot dermatitis, eyelid dermatitis, lichen simplex chronicus).
• Unfavorable prognostic factors for atopic dermatitis (in order of relative importance) include the following:
  • Persistent dry or itchy skin in adult life
  • Widespread dermatitis in childhood
  • Family history of atopic dermatitis
  • Associated bronchial asthma
  • Early age at onset
  • Female gender
• The objective when treating a patient for atopic dermatitis is control of exacerbations, not elimination of the disease. Using the above treatment modalities, patients and their families can hope to minimize the frequency and severity of outbreaks.

Patient Education

• Given the chronic nature of atopic dermatitis and patients' concerns about appearance, emotional support and psychological counseling may be helpful. Physicians need to be sensitive to the needs of patients and their families.

Multimedia

Media file 1: Typical atopic dermatitis on the face of an infant.

Media file 2: Flexural involvement in childhood atopic dermatitis.

Media file 3: Irritation around mouth of an infant with atopic dermatitis.

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Keywords

dermatitis, atopic dermatitis, atopy, atopic disease, dry skin, eczema, allergy, dermatitis treatment, dermatitis causes, dermatitis symptoms, ichthyosis vulgaris, keratosis pilaris, hand and foot dermatitis, keratoconus, chronic pruritic skin condition, fishlike scales, horny follicular papules, fissuring of the palms, fissuring of the soles, facial erythema, pityriasis alba, increased palmar linear markings, infraorbital fold, Dennie-Morgan line, pilaris, perioral pallor

Contributor Information and Disclosures

Author

Jamie Alison Edelstein, MD, Staff Physician, Department of Emergency Medicine, State University of New York, Kings County Hospital Center
Disclosure: Nothing to disclose.

Coauthor(s)

Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Robert M McNamara, MD, FAAEM, Chair and Professor, Department of Emergency Medicine, Temple University School of Medicine
Robert M McNamara, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Pennsylvania Medical Society, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Managing Editor

Mark W Fourre, MD, Program Director, Department of Emergency Medicine, Maine Medical Center; Associate Clinical Professor, Department of Surgery, University of Vermont School of Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
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The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Dara A Kass, MD, and Anthony J Ghidorzi, DO, to the development and writing of this article.

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